Postnatal nutritional iron deficiency impairs dopaminergic-mediated synaptic plasticity in the CA1 area of the hippocampus.

OBJECTIVES: Developmental iron deficiency (ID) has been shown to put children at risk for compromised learning and memory capacity, and it has also been shown to impair hippocampus-dependent forms of memory as well as hippocampal synaptic transmission. Catecholamines are known to play a pivotal role in memory consolidation, and studies have demonstrated that perinatal ID alters dopaminergic systems in various brain areas. It is not known, however, whether perinatal ID impairs dopaminergic synaptic plasticity in learning and memory structures such as the hippocampus. The objective of the present study was to examine dopaminergic-mediated synaptic efficacy in the hippocampus of mice subjected to an ID or control (CN) diet. METHODS: The present study used electrophysiological brain slice methods to examine dopaminergic-mediated synaptic efficacy in the hippocampus of mice subjected to an ID or CN diet from postnatal day (P) P0 through P20. Hippocampal brain slices were prepared in young (P26-30) and adult animals (P60-64). Synaptic efficacy was measured in CA1 neurons by examining population spike amplitude. Slices were treated with the dopaminergic agonist SKF-38393. RESULTS: Slices obtained from young and adult CN mice exhibited a long-lasting increase in synaptic efficacy as the result of SKF-38393 perfusion while the young and adult ID slices showed little or no increase. DISCUSSION: The present study demonstrates that postnatal ID produces long-lasting impairments in dopaminergic-dependent synaptic plasticity in the hippocampus. These impairments may play a role in the learning and memory deficits known to result from ID.

Effect of honey versus sucrose on appetite, appetite-regulating hormones, and postmeal thermogenesis.

OBJECTIVE: Increased per capita consumption of sweeteners may be responsible in part for the rising prevalence of obesity in the United States. Recent studies suggest that consumption of honey is not associated with this same obesogenic effect and may have beneficial effects neuro on body weight. The purpose of this study was to evaluate whether the meal-induced responses of ghrelin and peptide YY(3-36) (PYY(3-36)) and/or meal-induced thermogenesis differ following a honey- versus a sucrose-containing meal. METHODS: In a double-blind randomly assigned study, appetite hormones (ghrelin, PYY(3-36), leptin) and glycemic and thermic responses were evaluated following isoglucidic ∼450 kcal honey- or sucrose-containing breakfasts in 14 healthy, nonobese women (22 ± 3 y). Blood samples and hunger ratings were obtained at baseline and every 30 minutes for 240 minutes following the meal. Meal-induced thermogenesis was measured by indirect calorimetry. Ad libitum food intake was evaluated from a free-choice meal following the test meal. RESULTS: Honey consumption delayed the postprandial ghrelin response (p = 0.037), enhanced the total PYY (p = 0.007) response, and blunted the glucose response (p = 0.039) compared with consumption of the sucrose-containing meal. Meal-induced insulin response, hunger ratings, thermogenesis, and subsequent ad libitum food intake, however, did not differ (p > 0.10) between diet treatments. CONCLUSIONS: Alterations in meal-induced responses of ghrelin and PYY(3-36) but not meal-induced thermogenesis may be responsible in part for the potential "obesity protective" effect(s) of honey consumption. A blunted glycemic response may be beneficial for reducing glucose intolerance. Further research is required to determine if these findings hold true for obese individuals, for males, or with habitual consumption.